Page 174 - fbkCardioDiabetes_2017

150 DKD is Coronary Equivalent (Evidence And Remedy)

OTHER RISK FACTORS been shown to improve vascular reactivity and re-
duce markers of fibrinolysis and inflammation, and
they may reduce thickening of the carotid artery
wall. 22,23 They also reduce BP and may favorably af-
fect the lipid profile.

HYPERTENSION AND DYSLIPIDEMIA
Adding further fuel to fire are the two major risk fac-
tors: namely hypertension and dyslipidemia which
includes hypertriglyceridemia ; low levels of high
density lipoprotein (HDL) cholesterol, and elevated
levels of low density lipoprotein (LDL) cholesterol.
Blood pressure control has been shown to reduce the
risk of CVD and microvascular complications by one
third or more in patients with diabetes.In the UKP.
each 10 mm Hg reduction in systolic blood pressure
Table 1 : Risk factors for cardiovascular disease (CVD) in (SBP) was associated with a reduction of 15% in di-
T2 DM abetes-related deaths, 11% in MIs, and 13% in macro-
vascular complications.
Traditional risk factors for T2DM, including hypergly-
cemia, hypertension, and dyslipidemia, do not fully Role of Lipid Management: The characteristic pattern
account for the increased mortality from CVD in pa- of dyslipidemia associated with T2DM is one of el-
tients with T2DM. 15,16 Insulin resistance and a group evated triglyceride levels, low levels of HDL-C, and
of associated abnormalities, so-called non traditional elevated LDL-C consisting mostly of highly athero-
risk factors, have been identified as probable me- genic small dense LDL particles. Oxidative stress
diators and additional targets for treatment in these resulting from hyperglycemia further increases
patients (Table 1). 17,18 the risk of cardiovascular events in these patients.
For young patients (age ≤ 40 years) without overt
Role of Insulin Sensitizers CVD, the primary goal is an LDL-C level less than
Dandona and Aljada et al. have demonstrated that 100 mg/dL. More aggressive therapy is recommend-
insulin has anti- inflammatory and reactive oxygen ed for patients more than 40 years of age, those with
species (ROS) suppressive effects. In vitro studies additional cardiovascular risk factors, and those with
19
showed that insulin suppresses several inflammato- established CVD. In these high-risk groups, pharma-
ry mediators; adhesion molecules, chemokines and cotherapy is recommended, with the goal of achiev-
NFκB binding in human aortic endothelial cells. ing an LDL-C reduction of 30–40%, regardless of the
24
Metformin is a weak insulin sensitizer that works baseline level. In patients at high risk, including those
by reducing hepatic glucose output and increasing with acute coronary syndromes or a previous stroke
insulin action in muscle and fat. It was the first insu- or MI, a lower target of less than 70 mg/dL may be
lin sensitizer observed to reduce MIs and mortality appropriate, consistent with the NCEP ATP IIIoptional
in patients with diabetes. This effect was found to target for high-risk patients.
be greater in patients treated with metformin than
in those who achieved a similar degree of glyce- NON TRADITIONAL RISK FACTORS
mic control with noninsulin sensitizing agents. However, traditional risk factors for CVD do not fully
20
In a recent follow-up analysis of the UKPDS, patients account for the high prevalence of CVD and CVD
receiving metformin were found to have significant death in patients with CKD, especially DN. Recently,
reductions in the incidence of MI (33%; P < 0.01) and several non-traditional risk factors have been identi-
death from any cause (27%; P < 0.01), even 10 years fied. There are a number of novel risk factors for CVD

after the trial ended. 21 in patients with DN or CKD. These novel risk factors
may participate in inflammation and oxidative stress
Thiazolidinediones (TZDs) are more potent insulin in patients with diabetes or CKD.
sensitizers that work primarily by lowering insulin re-
sistance in peripheral tissues. These agents appear Homocysteine: Elevations of plasma homocysteine
to have a number of beneficial effects on non-tra- concentrations occur when the kidneys fail to excrete
ditional cardiovascular risk factors associated with homocysteine into the urine.Furthermore, defects of
insulin resistance. For example, these agents have any enzymes or cofactors involved in homocysteine

GCDC 2017